Lu-Qin Guo, Lan Zhou, Sheng-Nan Li, Juan Bai, Ling-Li Shi, Fang Hua, Peng Zhou
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引用次数: 0
Abstract
Kaempferol-3-O-rutinoside (KR) has an excellent cardioprotective effect, but its mechanism of action is not clear. Network pharmacology was used to predict the signaling pathways, whereas molecular docking was used for preliminary validation of KR binding to targets. AMI model rats with ligated left anterior descending coronary arteries were established. HE staining was used to detect pathological changes, and ELISA was used to detect the expression of TNF-α and IL-6. Network pharmacology results showed PI3K-AKT signaling pathway may be the main mechanism, and molecular docking predicted that KR could bind strongly to the PI3K and AKT. KR could significantly reduce cardiac pathological changes, decrease the level of TNF-α and IL-6, and enhance the mRNA and protein expressions of PI3K and AKT. KR ameliorates HF after AMI by enhancing the expressions of PI3K and AKT, which will be helpful in elucidating the mechanism of KR through multiple techniques.
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AP is an international, multidisciplinary journal devoted to pharmaceutical and allied sciences and contains articles predominantly on core biomedical and health subjects. The aim of AP is to increase the impact of pharmaceutical research in academia, industry and laboratories. With strong emphasis on quality and originality, AP publishes reports from the discovery of a drug up to clinical practice. Topics covered are: analytics, biochemistry, biopharmaceutics, biotechnology, cell biology, cell cultures, clinical pharmacy, drug design, drug delivery, drug disposition, drug stability, gene technology, medicine (including diagnostics and therapy), medicinal chemistry, metabolism, molecular modeling, pharmacology (clinical and animal), peptide and protein chemistry, pharmacognosy, pharmacoepidemiology, pharmacoeconomics, pharmacodynamics and pharmacokinetics, protein design, radiopharmaceuticals, and toxicology.
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